Mkb 10 alopecia areata. Alopecia, Diseases and treatment of folk and medicines

RCHD (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical Protocols of the Ministry of Health of the Republic of Kazakhstan - 2017

Alopecia totalis (L63.0), Alopecia universalis (L63.1), Alopecia areata (L63), Alopecia areata, unspecified (L63.9), Alopecia areata (BANDED FORM), Other alopecia areata (L63.8)

Dermatovenereology

general information

Short description

Approved
Joint Commission on the quality of medical services
Ministry of Health of the Republic of Kazakhstan
dated June 29, 2017
Protocol #24

Alopecia- this is a pathological hair loss caused by various effects on the hair follicle and clinically manifested by the formation of foci with a complete absence of hair on the head, beard, eyebrows, eyelashes and torso.

INTRODUCTION

ICD-10 code(s):

Protocol development date: 2017

Abbreviations used in the protocol:

Protocol Users: general practitioners, pediatricians, therapists, dermatovenereologists.

Evidence level scale:

A	High-quality meta-analysis, systematic review of RCTs, or large RCTs with a very low probability (++) of bias whose results can be generalized to an appropriate population.
B	High-quality (++) systematic review of cohort or case-control studies or High-quality (++) cohort or case-control studies with very low risk of bias or RCTs with low (+) risk of bias, the results of which can be generalized to the appropriate population .
C	Cohort or case-control or controlled trial without randomization with low risk of bias (+). The results of which can be generalized to the appropriate population or RCTs with a very low or low risk of bias (++ or +), the results of which cannot be directly generalized to the appropriate population.
D	Description of a case series or uncontrolled study or expert opinion.
GPP	Best Clinical Practice.

Classification

Classification :
By types:
· ordinary;
prehypertensive;
· atopic;
· autoimmune;
mixed.

By forms:
· local;
· ribbon-like;
subtotal;
total;
universal (malignant) form;
Alopecia areata with lesions of the nail plates.

By severity:
Light up to 25% of the area, single foci up to 3-5 cm in diameter;
average 25-50% of the area, foci 5-10 cm in diameter;
heavy up to 75% of the area.

With the flow:
acute;
subacute;
chronic.

According to the degree of activity:
progressing;
· stationary;
regressive.

Diagnostics

METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSIS AND TREATMENT

Diagnostic criteria

Complaints:
for hair loss.

Disease history:
Age of onset of the disease
connection with provoking factors;
The presence of this pathology in the next of kin, concomitant diseases.

Physical examination:
pathognomonic symptoms:
The presence of foci of alopecia with clear boundaries;
the presence of broken hair in the focus or along its edge;
The presence of light fluffy hair in the focus of growth

Laboratory research[ UD - V] :
· general blood analysis: increased number of platelets (endogenous intoxication);
Detection by microscopy of hair epilated from the focus of dystrophic proximal ends in the form of a “broken rope”;
microscopic examination for fungi;
Trichoscopy of the skin in the lesions;
· blood chemistry: determination of glucose, total protein, bilirubin cholesterol, creatinine, urea, ALAT, ASAT immunogram I and II levels; blood for the content of sex hormones (estrogen, progesterone), T-4, T-4, TSH.

Instrumental research: are not specific and mandatory, in case of detection of pathogenetic causal relationships, it is recommended:
· echoencephalography(to exclude pathological processes in the structure of the brain);
· radiography of the Turkish saddle(first of all, with total and universal forms to exclude volumetric formations);
· rheovasography of cerebral vessels or dopplerography of the vessels of the head and neck.

Indications for expert advice:
consultation of a therapist - in the presence of concomitant therapeutic pathology that worsens the course of the skin process;
consultation of a neuropathologist - to establish pathogenetic cause-and-effect relationships of hair loss;
consultation of an endocrinologist - to establish the pathogenetic cause-and-effect relationships of hair loss;
· consultation of a psychotherapist - for medical and social rehabilitation.

Diagnostic algorithm:(scheme)

Differential Diagnosis

Differential diagnosis and rationale for additional studies:

*Diagnosis*	*Rationale for*	*Surveys*	*Criteria*
	*differential*		*exclusion of the diagnosis*
	*diagnostics*
Trichotillomania	Foci of bizarre outlines, with uneven contours, often with the preservation of hair within the foci of alopecia, with the absence of vellus and a zone of loose hair.	Diagnosis is based on the histology of the biopsy - (hemorrhages and ruptures of the membranes, the absence of hair in the telogen phase.	1. The disease refers to disorders of the patient's habits and drives; 2. Noticeable loss of hair after repeated unsuccessful attempts to suppress the desire to pull them out; 2. Among patients, females aged 11-16 years predominate; 3. Areas of baldness tend to be symmetrical
Mycosis of the scalp	An inflammatory ridge is found along the periphery of the focus and the presence of hair stumps, broken off at a level of 2-3 mm from the skin surface.	To confirm the diagnosis, a microscopic examination is carried out for mycosis; drusen of fungi are detected inside and outside the hair shaft.	1. Most common in children and adolescents 2. On the scalp, rounded foci with moderate hyperemia, skin peeling and hair breaking at the level of 1-2 or 5-6 mm from the skin level are found. 3. Glow under a Wood's fluorescent lamp
Toxic alopecia	There is a clear relationship with the intake of cytostatics, anticoagulants, chemotherapy, psychotropic drugs and a severe infectious process.	The diagnosis is established on the basis of an anamnesis of the disease, a clinical picture in the form of focal or complete alopecia on the scalp and / or on the trunk	1. The disease often begins with severe symptoms of intoxication 2. At the same time, there may be involvement in the process of internal organs

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Treatment

Drugs (active substances) used in the treatment

Treatment (ambulatory)

PATIENTS OF TREATMENT AT THE OUTPATIENT LEVEL: all patients with this diagnosis are treated at the outpatient level.

Non-drug treatment:
Diet: table number 15, in the diet it is necessary to increase the amount of water consumed based on an increase in blood viscosity, signs of thickening of the peripheral blood).

Physiotherapy:
- narrow-band phototherapy using an excimer laser with a wavelength of 308 nm (C). The initial dose of laser radiation is 50 mJ/cm 2 less than the minimum erythemal dose; subsequently, the radiation dose is increased by 50 mJ/cm 2 every two sessions. The affected area is treated 2 times a week, no more than 24 sessions.

In severe forms of GA- PUVA therapy (C). Psoralen and its derivatives are used at a dose of 0.5 mg per kg of body weight 2 hours before the procedure. Irradiation dose - with a gradual increase from 1 J per 1 cm 2 to 15 J per 1 cm 2.

Medical treatment: the use of these drugs can be presented in the form of various treatment options, depending on the form (the indications for choosing this treatment method are indicated in the note). For example, the choice of systemic corticosteroids is necessary for severe forms of alopecia - total or rapidly progressive subtotal in adults and children. Topical corticosteroids (creams, ointments, lotions) are used starting from the focal form of alopecia in combination with vitamins, trace elements and immunomodulators, the duration of therapy is from 4 to 8 weeks. In the absence of the effectiveness of topical corticosteroids, peripheral vasodilators, dithranol, physiotherapy (PUVA) and systemic corticosteroids (standard therapy or pulse therapy) are connected.

When identifying the role of the immune system in the development of alopecia areata, immunosuppressive drugs are used - cyclosporine, methotrexate. Prescribing drugs mainly in individuals with long-term total alopecia, with a tendency to relapse and unresponsive to traditional therapy.

If the patient is prone to depression and emotional lability, consultation with a psychologist or psychiatrist is recommended.
It should be noted that the best option for patients with a single focus of alopecia is observation tactics, because. In 80% of patients with single patches present for less than a year, the alopecia spontaneously regresses.

List of Essential Medicines(having a 100% cast chance):

medicinal group	Medicines	Indications	Dosage, method of application	Level of Evidence	Note
Topical glucocorticosteroids	Prednisolone		cream, ointment 0.5% 2 times a day	WITH	In order to normalize local immunity, relieve inflammation
	Betamethasone valerate	All forms of alopecia areata, with the exception of universal	cream 0.1% 2 times a day	WITH
	Betamethasone dipropionate	All forms of alopecia areata, with the exception of universal	0.05% ointment 2 times a day	WITH
	Hydrocortisone butyrate	All forms of alopecia areata, with the exception of universal	cream 0.1% 2 times a day	IN
	Methylprednisolone aceponate	All forms of alopecia areata, with the exception of universal	cream 0.1% once a day	WITH
	Mometasone furoate	All forms of alopecia areata, with the exception of universal	cream 0.1% 1 time per day	WITH
	Betamethasone	All forms of alopecia areata, with the exception of universal	Ampoule 1.0 ml in / to 0.1 ml per 2 cm 2 every 4-6 weeks	WITH
	Diprospan (synthetic derivative of prednisolone)	All forms of alopecia areata, with the exception of universal	crystalline suspension, 1.0 ml ampoule in / to 0.1 ml per 2 cm 2 every 2 weeks	WITH
	triamcinolone acetonide,	All forms of alopecia areata, with the exception of universal	suspension for injection every 4-6 weeks in the form of multiple intradermal injections with an interval of 0.5-1 cm 0.1 ml is injected with a 30 gauge needle 0.5 inches long. The maximum dose per session should be 20 mg	IN
	clobetasol propionate,	For severe forms of alopecia	ointment 0.05% 2 times a day externally under an occlusive dressing with a duration of therapy up to 2 months.	IN
Peripheral vasodilator	Minoxidil	All forms of alopecia areata, with the exception of universal	Lotion (2-5% r-ramineoxidil) 2 times a day	A	The drug is a follicle stimulator
Dermatotropic agents	Dithranol	All forms of alopecia areata, with the exception of universal	Ointment 1 time per day	WITH	Side effects: inflammatory reactions and pigmentation of the surrounding healthy skin.
trace elements	zinc sulfate	All forms of alopecia areata	Powder 0.2 g once a day for 2 months	WITH
	zinc oxide	All forms of alopecia areata	powder 0.1 g 0.02 - 0.05 g (children) 2 times a day for 2 months
Systemic glucocorticosteroids*	Prednisolone		tablet 5 mg (course dose 40-60 mg)	WITH	according to indications, depending on the severity (total form of alopecia)
Systemic glucocorticosteroids*	Betamethasone	Subtotal form of alopecia and fulminant course	ampoules 1.0 ml 1 time in 7-10 days (from 4 to 6 procedures)	WITH
Antimetabolites	methotrexate	Severe form of alopecia	- tablets, solution for injection 15-30 mg once a week. orally or subcutaneously for 9 months; upon receiving a positive effect - extension of therapy up to 18 months. - solution for injection 15-30 mg once a week orally or subcutaneously in combination with prednisolone 10-20 mg per day day orally until the resumption of hair growth. - in the absence of a positive effect - the abolition of methotrexate.	WITH
Immunosuppressants. .	cyclosporine	Severe forms of alopecia	capsules, oral solution 2.5-6 mg per kg body weight per day orally for 2-12 months. Upon reaching positive clinical result, the dose is gradually reduced to complete abolition	WITH

Note: * - medicines, the evidence base for which is not sufficiently convincing today.

List of additional medicines:

medicinal group	Medicines	Indications	Dose and route of administration	Level evidence	Note
Drugs that improve peripheral circulation*	Deproteinized hemoderivative from calf blood	Common forms and relapsing course	ampoules 5.0 ml, 1 month		To stimulate hair growth by activating blood microcirculation under the skin
Potassium and magnesium supplements*	Orotic acid	Forms of alopecia against the background of potassium and magnesium deficiency, during therapy with systemic corticosteroids	tablets 0.5 3 times a day		for the entire course of hormone therapy, to reduce side effects

Surgery: No.

Further management:
rational nutrition with a high content of vitamins and microelements;
elimination of risk factors;
treatment of comorbidities;
courses of vitamin therapy, herbal medicine, adaptogens, lipotropic agents;
· Spa treatment.

Treatment effectiveness indicators:
· Criteria for evaluating the effectiveness of treatment:
0 points - no effect;
1 point - rare growth of vellus;
2 - growth of vellus and terminal hairs;
3 - terminal hair growth.
Restoration of the hair structure and overgrowth of all foci in all areas (scalp, mustache and beard areas in men and vellus hair on the body).

Hospitalization

INDICATIONS FOR HOSPITALIZATION WITH INDICATING THE TYPE OF HOSPITALIZATION

Indications for planned hospitalization: No.
Indications for emergency hospitalization: No.

Information

Sources and literature

Minutes of the meetings of the Joint Commission on the quality of medical services of the Ministry of Health of the Republic of Kazakhstan, 2017
1. 1) Skripkina Yu.K. Skin and venereal diseases [Text]: textbook - Moscow: GOETAR-Media, 2007.- 544 pp.: ill. 2) Federal clinical guidelines for the management of patients with alopecia areata. Moscow 2012 3) "Treatment of skin and venereal diseases". // Guide for doctors. THEM. Romanenko V.V. Kaluga, SL Afonin. Moscow 2006 4) Rational pharmacotherapy of skin diseases and sexually transmitted infections. Guide for practicing physicians. // Ed. A.A. Kubanova, V.I. Kisina. Moscow, 2005. 5) Evidence based (s3) guidelines for the treatment of androgenetic alopecia in women and in men // 2006 British Association of Dermatologists, British Journal of Dermatology, 149, 692–699. http://www.turkderm.org.tr/pdfs/S3_guideline_androgenetic_alopecia.pdf 6) Guidelines Guidelines for the management of alopecia areata // Accepted for publication 17 April 2007. 7) The therapeutic effect and the changed serum zinc level after zinc supplementation in alopecia areata patients who had a low serum zinc level. Park H, Kim CW, Kim SS, Park CW. // Ann Dermatol. 2009 May;21(2):142-6. Epub 2009 May 31. 8) Combination of topical garlic gel and betamethasone valerate cream in the treatment of localized alopecia areata: a double-blind randomized controlled study. // Indian J Dermatol Venereol Leprol. 2007 Jan-Feb;73(1):29-32. 9) Evidence based (s3) guidelines for the treatment of androgenetic alopecia in women and in men 2005 British Association of Dermatologists, British Journal of Dermatology.-149.-692–699 http://www.turkderm.org.tr/pdfs /S3_guideline_androgenetic_alopecia.pdf. 10) Wolff H, Fischer TW, Blume-Peytavi U, - DtschArzteblInt - May 27, 2016; 113(21); 377-86 11) Messenger AG, McKillop J, Farrant P, McDonagh AJ, Sladden M. British Association of Dermatologists" guidelines for the management of alopecia areata 2012. Br J Dermatol. 2012 May;166(5):916-26. 12) Gilhar A1, Etzioni A, PausR, "Published April 19, 2012. The New England journal of medicine, Volume 366, Issue 16; Pages 1515-25. 13) Gilhar A, Etzioni A, Paus R, - N. Engl J. Med. - April 19, 2012; 366 (16); 1515-25 14) Stefanato C. M. Histopathology of alopecia: a clinicopathological approach to diagnosis. Histopathology 2010; 56, 24-38. 15) Inui S., Nakajima T ., Nakagawa K., Itami S. Clinical significance of dermoscopy in alopecia areata: analysis of 300 cases Int J Dermatol 2008 Jul;47 (7): 688-93.16) Jain N, Doshi B, Khopkar U, - Int J Trichology - October 1, 2013; 5 (4); 170-8 17) Finner AM, Otberg N, Shapiro J, - DermatolTher - July 1, 2008; 21 (4); 279-94 18) Olsen E. A., Messenger A. G., Shapiro J., Bergfeld W.F., Hordinsky M.K., Roberts J.L., Stough D., Washenik K., Whiting D.A. Evaluation and treatment of male and female pattern hair loss // J. Am. Acad. Dermatol. - 2005. - Vol. 52(2). - P. 301-311. 19) Lee WS, Lee HJ, Choi GS, Cheong WK, Chow SK, Gabriel MT, Hau KL, Kang H, Mallari MR, Tsai RY, Zhang J, Zheng M, - J EurAcadDermatolVenereol - August 1, 2013; 27 (8); 1026-34 20) Scarinci F, Mezzana P, Pasquini P, Colletti M, Cacciamani A, - CutanOculToxicol - June 1, 2012; 31(2); 157-9. 21) Al-Mutairi N. 308-nm excimer laser for the treatment of alopecia areata. DermatolSurg 2007;33:1483-1487. 22) Al-Mutairi N. 308-nm excimer laser for the treatment of alopecia areata in children. PediatrDermatol 2009; 26:547-50. 23) Zakaria W, Passeron T, Ostovari N, Lacour JP, Ortonne JP. 308-nm excimer laser therapy in alopecia areata. J Am AcadDermatol 2004:51:837-838. 24) Raulin C, Gundogan C, Greve B, Gebert S. Excimer laser therapy of alopecia areata - side-byside evaluation of a representative area. JDtschDermatolGes 2005:3:524-526. 25) Gundogan C, Greve B, Raulin C. Treatment of alopecia areata with the 308-nm xenon chloride excimer laser: case report of two successful treatments with the excimer laser. Lasers SurgMed 2004:34:86-90. 26) Claudy AL, Gagnaire D. PUVA treatment of alopecia areata. Arch Dermatol 1983; 119:975-8. 27) Lassus A, Eskelinen A, Johansson E. Treatment of alopecia areata with three different PUVA modalities. Photodermatology 1984; 1:141-144. 28) Van der Schaar WW, Sillevis Smith JH. An evaluation of PUVA therapy for alopecia areata. Dermatologica 1984; 168:250-252. 29) Mitchell AJ, Douglass MC. Topical photochemotherapy for alopecia areata. J Am AcadDermatol 1985; 12:644-649. 30) Taylor CR, Hawk JL. PUVA treatment of alopecia areatapartialis, totalis and universalis: audit of 10 years’ experience at St John’s Institute of Dermatology. Br J Dermatol 1995;133:914-918. 31) Healy E, Rogers S. PUVA treatment for alopecia areata - does it work? A retrospective review of 102 cases Br J Dermatol 1993; 129:42-44. 32) Gupta AK, Ellis CN, Cooper KD et al. Oral cyclosporine for the treatment of alopecia areata. A clinical and immunohistochemical analysis. JAMAcadDermatol 1990; 22:242-50. 33) Fiedler-Weiss VC. Topical minoxidil solution (1% and 5%) in the treatments of alopecia areata. 34) Coronel-Perez IM, Rodriguez-Rey EM, Camacho-Martinez FM. Latanoprost in the treatment of eyelash alopecia in alopecia areatauniversalis. J EurAcadDermatolVenerol 2010; 24:481-5; 35) Faghihi G, Andalib F, Asilian A. The efficacy of latanoprost in the treatment of alopecia areata of eyelashes and eyebrows. Eur J dermatol 2009: 19:586-7. 36) Acikgoz G, Caliskan E, Tunca M. The effect of oral caclosporine in the treatment of severe alopecia areata. 37) Messenger AG, McKillop J, Farrant P, McDonagh AJ, Sladden M. British Association of Dermatologists’ guidelines for the management of alopecia areata 2012. British Journal ofDermatology 2012; 166:916-926. 38) Joly P. The use of methotrexate alone or in combination with low doses of oral corticosteroids in the treatment of alopecia totalis or universalis. J Am AcadDermatol 2006; 55:632-636. 39) Royer M, Bodemer C, Vabres P, et al. Efficacy and tolerance of methotrexate in severe childhood alopecia areata. Br J Dermatol 2011;165(2):407-10. 40) Gupta AK, Ellis CN, Cooper KD et al. Oral cyclosporine for the treatment of alopecia areata. A clinical and immunohistochemical analysis. JAM AcadDermatol 1990; 22:242-50. 41) Acikgoz G, Caliskan E, Tunca M. The effect of oral caclosporine in the treatment of severe alopecia areata.

Information

ORGANIZATIONAL ASPECTS OF THE PROTOCOL

List of developers:
1) Batpenova Gulnar Ryskeldievna - Doctor of Medical Sciences, Professor, Head of the Department of Dermatovenereology of JSC "Astana Medical University".
2) Dzhetpisbayeva Zulfiya Seytmagambetovna - Candidate of Medical Sciences, Associate Professor of the Department of Dermatovenereology of JSC "Astana Medical University".
3) Tarkina Tatyana Viktorovna - Doctor of Medical Sciences, Associate Professor of the Department of Dermatovenereology of JSC "Astana Medical University".
4) Tsoi Natalya Olegovna - PhD, assistant of the Department of Dermatovenereology of JSC "Astana Medical University".
5) Mazhitov Talgat Mansurovich - Doctor of Medical Sciences, Professor of the Department of Clinical Pharmacology and Internship of JSC "Astana Medical University", clinical pharmacologist.

Indication of no conflict of interest: absent

Reviewers:
1) Nurmukhambetov Zhumash Naskenovich - Doctor of Medical Sciences, Professor of the Department of Immunology and Dermatovenerology of the State Medical University of Semey.

Conditions for revision of the protocol: revision of the protocol 5 years after its publication and from the date of its entry into force or in the presence of new methods with a level of evidence.

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Alopecia areata (AA) is a chronic organ-specific autoimmune inflammatory disease with a genetic predisposition, characterized by damage to the hair follicles and sometimes the nail plates (in 7-66% of patients), persistent or temporary non-scarring hair loss.

Etiology and epidemiology

The basis of the development of the disease is assumed to be a local autoimmune mechanism of damage to the hair follicle, which leads to a violation of the immune tolerance of the cells that form the follicle and the termination of specific reception from its hair papilla.

The incidence and prevalence of HA depend on geographical and ethnic differences, as well as on the immunogenetic background of patients. The disease affects both sexes.

The predisposition to GA is genetic. 10-20% of patients have a family history of the disease, and the true incidence of the disease is probably even higher, since mild cases may go unnoticed. Genetic predisposition is polygenic in nature. GA has been associated with certain HLA class II alleles, especially with DQB1*03 and DRB1*1104. HLA alleles DQB1*0301(HLA-DQ7) and DRB1*1104 (HLA-DR11) may be associated with total and universal alopecia.

The trigger factors for the disease can be stress, vaccination, viral diseases, infectious diseases, taking antibacterial drugs, anesthesia, etc.

Conditions associated with GA.

Autoimmune thyroid diseases are observed in 8-28% of patients, while the presence of thyroid antibodies in the blood has no clinical correlation with the severity of HA. Vitiligo is observed in 3-8% of patients with GA. Atopy compared with the general population is recorded in patients with GA 2 times more often.

Relatives of patients with GA have an increased risk of developing type 1 diabetes; on the contrary, the incidence rate in the patients themselves compared with the general population may be lower. Patients with GA have a high rate of mental illness, especially anxiety and depressive disorders.

The incidence of GA is 0.7-3.8% of patients seeking help from a dermatologist. Risk of occurrence
disease during life is 1.7%. GA occurs equally in both men and women. The first focus of alopecia appears in 20% of patients in childhood, in 60% of patients under the age of 20, in 20% of patients over the age of 40.

Classification

L63.0 Alopecia total
L63.1 Alopecia universalis
L63.2 Nesting baldness (ribbon form)
L63.8 Other alopecia areata

Symptoms of alopecia areata

Depending on the volume and type of baldness, the following clinical forms of GA are distinguished:

local (limited);
subtotal;
total;
universal.

Other forms of GA are:

multifocal (network) location of alopecia areas;
ophiasis;
inverse ophiasis (sisapho);
diffuse form.

With a local (limited) form of GA, one or more clearly defined rounded foci of alopecia are determined on the scalp.

In the subtotal form of HA, more than 40% of hair is absent on the scalp.

With ophiasis, alopecia foci have a ribbon-like shape, cover the entire marginal zone of hair growth in the occipital and temporal regions.

With inverse ophiasis (sisapho), ribbon-shaped alopecia foci spread to the fronto-parietal and temporal regions.

The diffuse form of GA is characterized by partial or complete diffuse hair thinning on the scalp.

In the total form of HA, there is a complete loss of terminal hair on the skin of the scalp.

In the universal form of GA, hair is absent on the skin of the scalp, in the area of eyebrow and eyelash growth, and on the skin of the body.

Stages of the pathological process

Active (progradient, progressive) stage.

Subjective symptoms are usually absent, some patients may complain of itching, burning or pain in the affected area. Typical lesions are round or oval areas of non-scarring alopecia with unchanged skin color. Rarely observed foci of moderate red or peach color. Proximally narrowed and distally wide exclamation mark-shaped hair is a characteristic feature often seen in the affected area or around its periphery. In the active phase of the disease at the borders of the lesions, the hair tension test may be positive - the zone of "loose hair". The boundary of the zone does not exceed 0.5-1 cm.

GA can spread to almost any area of the scalp, but in about 90% of patients, the scalp is affected. At the initial stage, the disease does not affect gray hair.

stationary stage.

Around the focus of alopecia, the zone of "loose hair" is not defined, the skin in the focus is unchanged.

stage of regression.

In the focus of alopecia, there is a growth of vellus - vellus depigmented hair, as well as a partial growth of terminal pigmented hair. When hair regrows, the original hair is usually hypopigmented, but over time, the color usually returns.

In patients with HA, specific dystrophic changes in the nails can be observed: punctate ulceration of the nails, trachyonychia, Bo lines, onychorrhexis, thinning or thickening of the nails, onychomadesis, koilonychia, punctate or transverse leukonychia, red spotted lunulae.

Up to 50% of patients, even without treatment, recover within a year (spontaneous remission). At the same time, 85% of patients have more than one episode of the disease. With the manifestation of HA before puberty, the probability of developing total alopecia is 50%. With total / universal alopecia, the probability of complete recovery is less than 10%.

The prognosis is aggravated by the early age of onset of the disease, its duration, family history, the presence of concomitant atopy and other autoimmune diseases.

Diagnosis of alopecia areata

The diagnosis is made on the basis of the clinical picture of the disease:

the presence on the skin of foci of alopecia with clear boundaries;
the presence of hair stumps in the focus in the form of an exclamation mark and a “loose hair zone” at the border of the focus (active stage);
detection during microscopic examination of dystrophic proximal ends epilated from the focus of hair in the form of a “broken rope”;
the presence in the focus of growth of light fluffy hair (in the stage of regression); sometimes on one edge of the hearth there are fragments of hair in the form of an exclamation mark, and on the opposite side there is a growth of vellus;
detection of signs of onychodystrophy during examination of the nails: thimble-shaped indentations, longitudinal striation, changes in the free edge in the form of wavy patterns;
detection during trichoscopy (dermatoscopy of the scalp) of "yellow dots", cadaverized hair, hair in the form of exclamation marks.

In case of a doubtful diagnosis, as well as before prescribing treatment, it is recommended to conduct laboratory tests:

microscopic examination of the skin and hair for the presence of pathogenic fungi;
microscopic examination of hair epilated from the marginal zone of the focus (detection of dystrophic hair ends - a sign pathognomonic for GA);
histological examination of a fragment of the skin of the scalp. Histologically, GA is characterized by an inflammatory infiltrate consisting mainly of T cells in and around the bulbs of anagen hair follicles. However, the histopathological signs of GA depend on the stage of the disease; in the case of a chronic course of the disease, classical signs may be absent;
clinical blood test;
serological studies to exclude lupus erythematosus and syphilis;
determining the level of cortisol in the blood (when planning treatment with glucocorticoid agents of systemic action - before treatment and 4 weeks after its completion);
biochemical blood test: ALT, AST, total protein, bilirubin, cholesterol, blood sugar, alkaline phosphatase (if toxic alopecia is suspected, and also before prescribing photochemotherapy using photosensitizers inside);
survey radiography of the skull (to exclude volumetric formations in the area of the Turkish saddle);
a blood test for thyroid hormones (free T3, free T4, TSH, AT to TPO, AT to TG) to exclude thyroid pathology and prolactin to exclude prolactinemia.

According to indications, consultations of other specialists are appointed: a neurologist, an endocrinologist, a psychotherapist.

Differential Diagnosis

Differential diagnosis is carried out with trichotillomania, diffuse toxic alopecia, trichophytosis of the scalp, cicatricial alopecia.

With trichotillomania, alopecia foci are irregularly shaped, usually located in the temples, crown, eyebrows, eyelashes. In the central part of the focus, the growth of terminal hair is often observed. In the focus, the hair can be broken off at various lengths. Microscopic examination determines the hair roots in the anagen or telogen stage, there are no dystrophic hairs.

Diffuse toxic alopecia is usually associated with acute toxic conditions: poisoning with salts of heavy metals, chemotherapy, taking cytostatics, prolonged temperature rise to 39 ° C and above.

With trichophytosis of the scalp, during the examination, an inflammatory ridge is found along the periphery of the focus and the presence of "stumps" - hair broken off at a level of 2-3 mm from the skin surface. The disease may be accompanied by inflammation and desquamation, which, as a rule, is not observed in GA. Microscopic examination of hair fragments for fungi reveals fungal drusen inside or outside the hair shaft.

With cicatricial alopecia, the skin in the lesion is shiny, the follicular apparatus is not expressed. Clinical manifestations of cicatricial alopecia sometimes cause difficulties in diagnosis, in which case a histological examination is recommended.

In children with congenital single area of alopecia in the temporal zone, a differential diagnosis with temporal triangular alopecia should be carried out.

In rare cases of GA with damage to the frontal hairline and temporal zone, frontal fibrous alopecia should be excluded - cicatricial hair loss, affecting mainly women in the postmenopausal period. The disease may be accompanied by perifollicular erythema and scaling, which are not observed in GA.

Treatment for alopecia areata

Treatment regimens

Medical therapy

Systemic therapy in severe forms of GA.

Glucocorticosteroid preparations.

prednisolone
methylprednisolone

Antimetabolites

methotrexate

Immunosuppressants.

cyclosporine

Systemic therapy for local (limited) GA:

zinc sulfate

External therapy in severe forms of GA.

minoxidil, solution 5%
clobetasol propionate, ointment 0.05%

External therapy for local (limited) GA: - Intralesional administration of glucocorticosteroid drugs.

triamcinolone acetonide
betamethasone dipropionate (2 mg)
Minoxidil
minoxidil, solution 2%
minoxidil, solution 5%

Topical glucocorticosteroid drugs:

fluocinolone acetonide cream 0.25%
betamethasone valerate, foam 0.1%, cream
betamethasone dipropionate, lotion 0.05%, cream
clobetasol propionate cream 0.05%
hydrocortisone butyrate, cream 0.1%, emulsion
mometasone furoate cream 0.1% lotion
methylprednisolone aceponate, cream 0.1%, emulsion

Analogues of prostaglandin F2a are used in the formation of alopecia in the area of eyelash growth (C).

latanoprost, solution 0.03%
bimatoprost, solution 0.03%

Non-drug therapy

In local GA - narrow-band phototherapy using an excimer laser with a long wavelength of 308-nm

In severe forms of HA - PUVA therapy (C). Psoralen and its derivatives are used at a dose of 0.5 mg per kg of body weight

Indications for hospitalization

None.

Requirements for treatment outcomes

Resurgence of hair growth in the foci of alopecia.

Tactics in the absence of effects from treatment

Patients with prolonged absence of eyebrows may be offered dermatography or medical tattooing. Hair prostheses, wigs, hairpieces and other extensions are recommended for patients with hypertension for the period of therapy or in the absence of the effect of treatment.

Prevention

There are no methods of prevention.

If you have any questions about this disease, then contact the dermatovenereologist Adaev Kh.M:

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Medicine knows various types of diseases of the hair and scalp. One of the varieties of such diseases is focal alopecia. However, not everyone knows what this medical term means. We will tell you about this and much more in this article.

What is alopecia areata?

Alopecia areata (alopecia areata) - this disease is associated with damage to the cells of the hair root system and is characterized by the sudden appearance of one or more foci of oval or rounded baldness. In places of bald patches there is no itching or pain, the skin is even in natural color.

Alopecia areata is rare and can both appear and disappear completely unexpectedly for the patient. Often the symptoms of the disease go away on their own, without any treatment. However, there are relapses of this disease.

If the patient first had a small single foci of baldness, then it is likely that it will grow on its own, you just need to calmly wait and follow it for about three months.

In the case when alopecia areata begins to develop into a multifocal form, the patient should seek the advice of a doctor.

It happens that this disease begins with a small spot of baldness, then it grows into rather large bald patches, or the same spots can appear not only on the scalp, but also in any other places on the body. This form of alopecia areata is called subtotal.

When alopecia areata has developed into a total or universal stage, patients experience hair damage throughout the body, which is also accompanied by damage to the nail plates. In such complex cases, only a doctor can establish the correct diagnosis and prescribe effective methods of treatment, but for this the patient needs to undergo a complete examination and establish the causes of this disease.

Mature hair loss usually leads to a decrease in the density of the hairline and, quite rarely, to total alopecia. There are a lot of reasons for mature hair loss, for example, due to physiological changes in the body during pregnancy, alopecia may occur after childbirth. Long-term use of retinoids, oral contraceptives and drugs that slow down blood clotting, especially in combination with constant stressful situations and endocrine disorders, quite often cause alopecia. Lack of iron, zinc and other malnutrition in the body also adversely affects the density of the hairline.
As a rule, alopecia begins gradually with the appearance of small bald patches in the parietal or frontal part of the head, the skin acquires a glossy sheen, atrophy of the hair follicles is observed, in the center of the foci one can find single long hair that has not changed in appearance.
If the cause of alopecia is the loss of growing hair, then over time this can lead to complete hair loss. Pathogenetically, this type of alopecia is caused by mycoses, radiation therapy, poisoning with bismuth, arsenic, gold, thallium and boric acid. Hair loss and alopecia may be preceded by anticancer therapy using cytostatics.
Androgenetic alopecia is observed mainly in men, it begins to appear after puberty and is formed by the age of 30-35. The development of alopecia in this case is associated with an increased amount of androgenic hormones, which is due to hereditary factors. Clinically, androgenetic alopecia is manifested by the replacement of long hair with vellus, which over time become even shorter and lose pigment. Initially, symmetrical bald patches appear in both temporal areas with a gradual involvement of the parietal zone in the process. Over time, bald patches merge due to peripheral growth.
Scarring alopecia, in which hair loss is accompanied by the appearance of shiny and smooth areas of the scalp, is characterized in that such areas do not contain hair follicles. The cause of this type of alopecia may be a congenital anomaly and defects of the hair follicles. But much more often, infectious diseases, such as syphilis, leprosy, and herpes infections, lead to cicatricial alopecia. Changes in the ovaries and pituitary gland in the form of hyperplasia and polycystosis, basal cell carcinoma, long-term use of steroid drugs also provoke cicatricial alopecia. Exposure to aggressive chemicals, burns, frostbite of the scalp are the most common exogenous causes of cicatricial alopecia.
Alopecia areata, when areas of baldness are not accompanied by scarring and are located in the form of rounded foci of different sizes, appear suddenly. The causes of alopecia areata are not known, but meanwhile, areas with alopecia tend to grow peripherally, which can lead to total hair loss. Most often, alopecia areata occurs on the scalp, but the process of baldness can affect the area of the beard, mustache, eyebrows and eyelashes. Initially, foci of alopecia are small, up to 1 cm in diameter, the skin condition is not changed, but slight hyperemia can sometimes be observed.
The mouths of hair follicles in the affected area are clearly visible. As the peripheral growth foci of alopecia acquire a scalloped character and merge with each other. In the circumference of the areas there is a zone of loose hair, which, with a slight impact, is easily removed, the hair in this zone at its root is devoid of pigment and ends in a club-shaped thickening in the form of a white dot. They got the name "exclamation mark hair". The absence of such hair indicates that alopecia areata has passed into the stationary stage and the end of the progression of hair loss. After a few weeks or months in the foci of alopecia, hair growth is restored. At first they are thin and colorless, but over time their color and texture become normal. The fact that hair growth has resumed does not exclude the possibility of relapses.
Seborrheic alopecia occurs in approximately 25% of cases of seborrhea. Baldness begins during puberty and reaches its maximum severity by 23-25 years. At first, the hair becomes greasy and shiny, outwardly looking like oiled. The hair sticks together in strands, and on the scalp there are tightly seated greasy yellowish scales. The process is accompanied by itching and seborrheic eczema often joins. Baldness begins gradually, at first the life of the hair is shortened, they become thin, thin and gradually long hair is replaced by vellus. As seborrheic alopecia develops, the process of hair loss begins to increase, and the bald spot becomes noticeable, it starts from the edges of the frontal zone towards the back of the head or from the parietal zone towards the frontal and occipital. The center of baldness is always bordered by a narrow band of healthy and tight-fitting hair.

Alopecia- absence or thinning of hair on the skin in places of their usual growth (more often on the scalp).

Code according to the international classification of diseases ICD-10:

L63- Alopecia areata
L64- Androgenetic alopecia
L65- Other non-scarring hair loss
L66- Scarring alopecia
Q84. 0 - congenital alopecia

Frequency

50% of men by the age of 50 have distinct signs of male pattern baldness. 37% of postmenopausal women note certain signs of alopecia.

Dominant age

the frequency of androgenetic alopecia increases in proportion to age; dermatomycosis of the scalp and traumatic alopecia more often occur in children.

Alopecia: Causes

Etiology

Mature hair loss: . After childbirth as a result of physiological changes in the body of a pregnant woman. Drugs (oral contraceptives, anticoagulants, retinoids, b-blockers, anticancer drugs, interferon [IFN]). Stress (physical or mental). Endocrine pathology (hypo - or hyperthyroidism, hypopituitarism). Alimentary factors (malnutrition, deficiency of iron, zinc). Loss of growing hair: . Fungal mycosis. X-ray therapy. Drugs (anticancer drugs, allopurinol, bromocriptine). Poisoning (bismuth, arsenic, gold, boric acid, thallium). cicatricial alopecia: . Anomalies of development and congenital malformations. Infections (leprosy, syphilis, herpes infection, cutaneous leishmaniasis). Basal cell carcinoma. epidermal nevi. Exposure to physical factors (acids and alkalis, extreme temperatures [burns, frostbite], exposure to radiation). Cicatricial pemphigus. Lichen planus. Sarcoidosis. Androgenic alopecia: . Hyperplasia of the adrenal cortex. Polycystic ovaries. Hyperplasia of the ovaries. Carcinoid. hyperplasia of the pituitary gland. Drugs (testosterone, danazol, ACTH, anabolic steroids, progesterone). nesting alopecia. Etiological factors are unknown, an autoimmune nature is possible; inherited forms are described. traumatic alopecia: . Trichotillomania (irrepressible urge to pull out one's own hair). Damage due to braiding or tight knotting. Dermatomycosis of the scalp: . Fungi of the genus Microsporum. Fungi of the genus Trichophyton.

Genetic Aspects

At least 90 inherited diseases and syndromes are known to be accompanied by alopecia. congenital alopecia with keratosis of the palms and soles (104100, Â) . Congenital total alopecia(*104130, Â): associated with giant pigmented nevi, periodontitis, convulsions, mental retardation. nesting alopecia(104000, Â) . Family alopecia(transformation anagen - telogen, foci of alopecia, 104110, Â) . Total alopecia(203655, 8p12, HR gene, r) . Various degrees of hypotrichosis, up to the complete absence of hair, are characteristic of hereditary ectodermal dysplasia (see Ectodermal dysplasia).

Risk factors

Hair loss in family history. Physical or mental stress. Pregnancy. nesting alopecia- Down's syndrome, vitiligo, diabetes.

Types

Mature hair loss (telî gen effluvium) - diffuse hair loss, leading to a decrease in hair density, but not to complete baldness. Loss of growing hair (anà gen effluvium) - diffuse hair loss, including growing hair, with possible complete baldness. cicatricial alopecia- the presence of shiny smooth areas on the scalp that do not contain hair follicles. Androgenic alopecia- hair loss, usually developing in both sexes; possibly due to the effect on the cells of the hair follicles of male sex hormones. nesting alopecia(circular alopecia) - acquired hair loss in the form of rounded foci of various sizes in certain areas of the scalp, eyebrows, beard area, not accompanied by scarring. traumatic alopecia- hair loss in certain areas of the skin due to chronic trauma, not accompanied by scarring in the early stages. Dermatomycosis of the scalp (tinea capitis) - the presence of limited foci with the absence of hair on the scalp, possibly combined with an inflammatory reaction; caused by a fungal infection.

Alopecia: Signs, Symptoms

Clinical picture

Hair loss. With ringworm of the scalp - itching, peeling, inflammation. With ringworm of the scalp and traumatic alopecia - hair breaking. With alopecia areata: sudden appearance on the scalp, face of several rounded foci of complete hair loss without any other changes; hair on the periphery of the foci is easily pulled out; foci can grow, merge and lead to total alopecia.

Alopecia: Diagnosis

Laboratory research

Investigation of the functions of the thyroid gland. Complete blood count (to identify possible disorders of the immune system). Levels of unbound testosterone and dihydroepiandrosterone sulfate in women with androgenetic alopecia. Plasma ferritin concentration. Von Wassermann reaction to rule out syphilis. The number of T - and B - lymphocytes (sometimes reduced in patients with alopecia areata).

Special Studies

Hair pulling test: Gently pulling (without effort) on the hair shaft to remove it; positive (hair is easily removed) with alopecia areata. Microscopic examination of the hair shaft. Examination of foci of peeling with potassium hydroxide; positive for ringworm of the scalp. The use of antifungal drugs can lead to false positive results. Examination of foci of peeling for the presence of fungi. Biopsy of the scalp with conventional microscopy and direct immunofluorescent examination allows diagnosing ringworm of the scalp, diffuse alopecia areata and scarring alopecia that developed against the background of SLE, lichen planus and sarcoidosis.

Alopecia: Treatment Methods

Treatment

Tactics of conducting

Loss of mature hair. Hair loss maximum 3 months after the causative effect (drug, stress, alimentary factors); after the cause is eliminated, hair growth is quickly restored. Loss of growing hair. Hair loss begins a few days or weeks after the causative effect, hair growth is restored after the cause has been removed. cicatricial alopecia. The only effective method of treatment is surgical (skin flap transplantation or excision of scarring areas). Androgenic alopecia. After 12 months of topical application of minoxidil, 39% of patients noted hair growth of varying severity. An alternative method of treatment is surgery. nesting alopecia. Usually the disease resolves on its own within 3 years without treatment, but relapses often occur. traumatic alopecia. The cure can come only after the cessation of hair-pulling. The intervention of a psychologist or psychiatrist may be required. Successful treatment includes drug therapy, behavior modification, and hypnosis. Dermatomycosis of the scalp: treatment is carried out for 6-8 weeks. Thorough washing of hands and laundering of hats and towels is required.

Drug therapy

Finasteride tablets. Good results have been obtained with various forms of alopecia. With androgenetic alopecia - minoxidil (2% r - r) for topical application. With alopecia areata. Sedatives, vitamins, irritating alcohol rubs. HA preparations for local use. In severe cases - photosensitizing drugs (beroxan) locally in combination with ultraviolet irradiation (UVI), HA orally. With ringworm of the scalp - griseofulvin (adults 250-375 mg / day, children 5, 5-7, 3 mg / kg / day) or ketoconazole 200 mg 1 r / day for 6-8 weeks.

Surgery

Skin transplant.

Course and forecast

Loss of mature and growing hair: permanent baldness rarely develops. cicatricial alopecia: hair follicles are constantly damaged. Androgenic alopecia: the prognosis and course depend on the treatment. nesting alopecia: spontaneous recovery is possible, but relapses are not uncommon, with a total form, the hair usually does not recover. traumatic alopecia: the prognosis and course depend on the success of the correction of the patient's behavior. Ringworm of the scalp: usually resolves completely.

Synonyms

Atrichia. Atrichosis. Baldness. Baldness

ICD-10. L63 Female alopecia. L64 Androgenic alopecia. L65 Other non-scarring hair loss. L66 Scarring alopecia. Q84. 0 Congenital alopecia